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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of exogenous insulin on oxidation of glucose and fatty acid were investigated in septic (n = 20) and control rats (n = 20). Sepsis was induced by ligation and puncture of the caecum. The rats received intravenous nutrition with glucose as a non-protein calorie for 27 hours. Ten rats in each group received insulin intravenously at a rate of 0.64U/kg/hr during the last 6 hours of the intravenous nutrition, U-14C-glucose or 1-14C-linoleic acid at a dose of 1.563 microCi each was injected as a bolus at the 21st hour of the intravenous nutrition. Cumulative 14CO2 production was measured for 6 hours after the injection of the radioactive substrates. 14CO2 production from both glucose and linoleic acid was inhibited by the sepsis. 14CO2 production from glucose was accelerated by exogenous insulin in the control rats, while it was not accelerated in the septic rats. Exogenous insulin did not affect 14CO2 production from linoleic acid in both the control and the septic rats. These results indicate that, under the condition of sepsis, lowering blood sugar level with exogenous insulin does not refLect an increase in oxidation of glucose.
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PMID:[Effects of exogenous insulin on oxidation of glucose and fatty acid in septic rats]. 266 30

The present study examined whether sepsis exacerbates the diabetes-induced peripheral and hepatic insulin resistance. Vascular catheters were placed in diabetic (70 mg/kg streptozotocin, 4-wk duration) and nondiabetic rats, and sepsis was produced by subcutaneous injections of live Escherichia coli. Basal glucose metabolism was determined with the use of [3-3H]glucose initiated 18 h after the first injection of bacteria. Thereafter, in vivo insulin action was assessed with the use of the euglycemic hyperinsulinemic clamp technique. Sepsis in nondiabetic rats produced a 57% reduction in the maximal responsiveness for the insulin-induced increase in total glucose utilization compared with nondiabetic nonseptic animals. Diabetes alone decreased both insulin sensitivity and responsiveness. When the septic insult was superimposed on the diabetic condition, the maximum responsiveness was unchanged compared with non-septic diabetic rats, but the 50% maximally efficient dose was reduced from 817 to 190 microU/ml, suggesting an improvement in insulin sensitivity. Sepsis did not alter the insulin-induced suppression of hepatic glucose output in either nondiabetic or diabetic animals. Sepsis increased the plasma concentrations of epinephrine, norepinephrine, glucagon, and corticosterone in both nondiabetic and diabetic rats; however, the elevation in catecholamines and glucagon was 65 to 250% greater in the diabetic animals. These results indicate that hypermetabolic sepsis produces peripheral insulin resistance in nondiabetic rats but does not worsen the preexisting insulin resistance in diabetic animals, despite the higher prevailing blood levels of glucagon and catecholamines.
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PMID:Sepsis-induced changes in in vivo insulin action in diabetic rats. 267 27

We have investigated the responsiveness of protein kinetics to insulin and the role of glucose oxidation rate as a mediator of the protein catabolic response to burn injury and sepsis by assessing the response of leucine and urea kinetics to a 5-h hyperinsulinemic euglycemic clamp with and without the simultaneous administration of dichloroacetate (DCA) (to further increase glucose oxidation via stimulation of pyruvate dehydrogenase activity) in eight severely burned and eight septic patients. Leucine and urea kinetics were measured by the primed-constant infusions of [1(-13)C]leucine and [15N2]urea. Compared with controls, basal leucine kinetics (flux and oxidation) were significantly elevated (P less than 0.01) in both groups of patients. Hyperinsulinemia elicited significant (P less than 0.05) decreases in leucine kinetics in both groups of patients. Consistent with this observation, hyperinsulinemia caused urea production to decrease significantly (P less than 0.05) in both patient groups. The administration of DCA to patients during hyperinsulinemia elicited a significant increase in glucose oxidation rate compared with the clamp rate (P less than 0.05), and the percent of glucose uptake oxidized increased from 45.5 +/- 5.5 to 53.5 +/- 4.8%; yet the response of leucine and urea kinetics to the clamp plus DCA was not different from the response to the clamp alone. These results suggest that the maximal effectiveness of insulin to suppress protein breakdown is not impaired and that a deficit in glucose oxidation or energy supply is probably not playing a major role in mediating the protein catabolic response to severe burn injury and sepsis.
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PMID:Role of insulin and glucose oxidation in mediating the protein catabolism of burns and sepsis. 267 28

The effect of sterile inflammation and sepsis on the release of lactate and amino acids by peripheral tissues was investigated in rats by removing the splanchnic organs (liver + small intestines) from the circulation and monitoring changes in blood metabolites over 30 min. Functional hepatectomy was performed in rats 5-7 days following the intraperitoneal introduction of a fecal-agar pellet (sterile vs. Bacteroides fragilis + E. coli). Lactate was significantly (P less than .05) increased in each of the conditions following hepatectomy but was raised to a significantly greater extent in sepsis (P less than .05). A similar response was observed for glutamine while alanine was only significantly (P less than .05) increased in sepsis following hepatectomy. Branched chain amino acids (BCAA) showed differential changes in sepsis compared to control. In control and sterile inflammation, functional hepatectomy was associated with significant decreases (P less than .05) in BCAA. In sepsis, BCAA were not decreased following hepatectomy and were significantly (P less than .05) elevated relative to control or sterile inflammation. Phenylalanine concentrations were not altered in control or sterile inflammation but were significantly elevated in sepsis (P less than .05). Insulin attenuated the accumulation of lactate and amino acids in fed control animals, following functional hepatectomy. However, in septic animals, insulin failed to prevent the rise in plasma lactate following hepatectomy.
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PMID:Role of extra-splanchnic organs in the metabolic response to sepsis: effect of insulin. 267 32

Sepsis and extensive burn injury produce clinical syndromes characterized in part by "insulin resistance," but it is unclear if these insulin resistant states are identical. To test if the maximal biological effectiveness of insulin is altered in septic or burned patients, eight septic patients and eight nonseptic patients recovering from severe burn injury were studied using the hyperinsulinemic eukalemic euglycemic clamp technique. Compared with bed-rested controls, the septic patients showed an insulin-induced plasma clearance of potassium, which was 183% higher (P less than .001), and a concomitant glucose clearance, which was 52% lower (P less than .001). Nonseptic burn patients also had a 91% increase in potassium clearance (P less than .05), but their maximal insulin-stimulated glucose uptake was not different from that of bedrested controls. When septic patients were compared with their nonseptic burned counterparts, there was no difference in potassium clearance in response to insulin, but glucose uptake by the septic patients was 47% lower (P less than .001). Insulin infusion completely suppressed hepatic glucose production in both septic patients and in nonseptic burn patients. The percent of whole body glucose uptake that was oxidized was not different between the septic patients and the nonseptic postburn patients in both the basal and insulin-stimulated states (38% and 51% v 38% and 42%, respectively). It is concluded that septic and postburn insulin resistance differ in that peripheral glucose uptake in sepsis, but not nonseptic burn injury, is refractory to pharmacologic insulin stimulation, whereas in both states insulin effectively stimulates potassium uptake.
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PMID:Differentiation between septic and postburn insulin resistance. 267 12

Circulating factors produced by the macrophages mediate skeletal muscle proteolysis in sepsis and trauma. This study was done to determine whether cytokines affect skeletal muscle metabolism in cancer. Using a method initially developed to measure proteolytic factors in sepsis and trauma, plasma from cachectic cancer patients, noncachectic cancer patients, and normal controls was tested for effects on normal rat skeletal muscle (soleus, extensor digitorum longus). The experimental design allows concomitant measurement of protein synthesis, by [14C]phenylalanine uptake, and protein degradation, by tyrosine release. Plasma from cancer patients caused no acceleration of protein degradation. Noncachectic cancer plasma acted synergistically with insulin to increase protein synthesis (P less than 0.05). These results indicate that a growth factor is present in the plasma of cancer patients who have not become cachexic. To our knowledge, this is the first documentation of a cancer plasma growth factor acting at the organ level to induce synthesis. Our data refute the theory that cancer cachexia is mediated by circulating proteolytic factors. In a separate experiment, purified human recombinant tumor necrosis factor (rTNF) was incubated with normal rat skeletal muscle. No changes were seen in synthesis or degradation rates. Skeletal muscle proteolysis does not appear to be directly induced by rTNF.
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PMID:Effect of cancer plasma on skeletal muscle metabolism. 268 6

The authors describe a term female, asphyxiated, small for gestational age (SGA) infant with documented hyperinsulinism and hypoglycemia occurring at approximately 45 hours of age. The hypoglycemia was refractory to a high rate glucose infusion and steroid administration but responded to diazoxide. The subsequent hospital course was complicated by right-sided heart failure and sepsis. With the onset of sepsis, a transient hyperglycemia was noted that required intermittent insulin therapy for 10 days. Hypoglycemia and hyperinsulinism reemerged and responded to diazoxide therapy. An attempt to discontinue diazoxide at age 6 months was aborted at 2 weeks when hyperinsulinism and hypoglycemia recurred. The infant required diazoxide for 7 more months, then she recovered without having any sequelae. The review of this uncommon hypoglycemia etiology in an SGA and asphyxiated infant and the merits of long-term diazoxide treatment are discussed.
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PMID:Prolonged hyperinsulinism and hypoglycemia. In an asphyxiated, small for gestation infant. Case management and literature review. 268 73

We reported a case of halothane-induced fulminant hepatitis with acute renal failure which developed 6 days after reexposure to halothane. The patient was a 58-year-old female. She had a history of liver dysfunction after exposure to halothane 6 years previously. She had surgical treatment of clubfoot under halothane anesthesia in other hospital. Preoperative physical examination and laboratory data were normal. On the 6th post-operative day she abruptly developed high fever and general fatigue. Next day, she was transferred to our hospital. At admission, fulminant hepatitis complicated with acute renal failure was diagnosed with severe liver and renal damage. She was immediately treated with plasma exchange, glucose-insulin therapy, and hemodialysis. Serum transaminase level returned to normal value within a week. However, despite repeated hemodialysis, renal function did not improve, and she died of P. aeruginosa sepsis on 28th day after the operation. It may be suggested that in this patient hypersensitivity to halothane has persisted during the six years.
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PMID:[A case of fulminant hepatitis after reexposure to halothane six years later]. 281 Jul 19

Because of its wide distribution in the organism, natural somatostatin (SRIF) demonstrates an ample spectrum of actions, involving mainly the central neuroendocrine system and the enteropancreatic area. In the former, this peptide may find its field of application in conditions characterized by excessive GH, TSH or ACTH secretion, depending on the central or peripheral cause of the inappropriate hormone control. The inhibitory effect of SRIF on gastrointestinal and pancreatic hormones may be useful in the management of tumors originating in this system and also in the treatment of inflammatory processes such as pancreatitis, in malignant diarrhea, and in gastrointestinal bleeding. A complex action of SRIF and its derivative on insulin release and glucose homeostasis may offer some advantages in the control of unstable diabetes. Dampening of organic functions in the upper digestive tract may also render SRIF and its analogues useful in the exploration of the gallbladder, gastric and pancreatic functions. The effect of such peptides on tissue growth and on the regulation of blood pressure are the subject of present investigations. Cytoprotection, an interesting aspect of SRIF application, is discussed elsewhere in this compendium. Finally, some comments on the possible use of SRIF as an additive to the conventional treatment of burns and sepsis close this review.
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PMID:Clinical applications of somatostatin. 290 Feb 4

The present study examined the purported exacerbating effect of sepsis on glucose metabolism in diabetes. Diabetes was induced in rats by an intravenous injection of 70 or 45 mg/kg streptozotocin. The higher dose produced "severe" diabetes, whereas the lower dose of streptozotocin produced a milder, "latent" diabetes. After a chronic diabetic state had developed for 4 wk, rats had catheters implanted and sepsis induced by intraperitoneal injections of live Escherichia coli. After 24 h of sepsis the blood glucose concentration was unchanged in nondiabetics and latent diabetics, but glucose decreased from 15 to 8 mM in the septic severe diabetic group. This decrease in blood glucose was not accompanied by alterations in the plasma insulin concentration. Glucose turnover, assessed by the constant intravenous infusion of [6-3H]- and [U-14C]glucose, was elevated in the severe diabetic group, compared with either latent diabetics or nondiabetics. Induction of sepsis produced a slight decrease in the glucose turnover in the severe diabetic group but did not alter turnover in the latent diabetics. The rate of glucose disappearance, used to quantitate the alterations in plasma glucose after an intravenous glucose tolerance test, was decreased in both groups of diabetics and was proportional to the severity of the diabetic state. Sepsis increased the rate of glucose disappearance in nondiabetic rats but had no effect in either group of diabetic animals. Sepsis also failed to alter the insulinogenic index, used to estimate the insulin secretory capacity, in diabetic rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Altered glucose kinetics in diabetic rats during gram-negative infection. 295 88


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